MCP-1 exerts the inflammatory response via ILK activation during endometriosis pathogenesis

Upendra Kumar Soni, Rupal Tripathi, Rajesh Kumar Jha
Life sciences · 2024 · vol. 353 , pp. 122902 · doi:10.1016/j.lfs.2024.122902 · PMID:39004271 · W4400612653
article OA: closed CC0 ⤵ 6 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This study investigated how MCP-1 contributes to endometriosis pathogenesis by activating ILK, revealing a key inflammatory pathway involved in the disease.

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Abstract

AIMS: MCP-1 has been shown to be elevated in endometriosis. ILK functions in several cellular events and interacts with MCP-1-signaling. In the current study, we evaluated the role of MCP-1-ILK signaling in human endometriotic cell's (Hs832(C).TCs) potential for colonization, invasion, adhesion, etc. and differentiation of macrophage along with inflammation in an endometriosis mouse model. MATERIALS AND METHODS: A mouse model of endometriosis with elevated levels of MCP-1 was developed by injecting MCP-1. We examined the migration, adhesion, colonization and invasion of Hs832(C).TCs in response to MCP-1-ILK signaling. We also examined the differentiation of THP-1 cells to macrophage in response to MCP-1-ILK signaling. KEY FINDINGS: We observed that MCP-1 increased Ser246 phosphorylation of ILK in Hs832(C).TCs and enhanced the migration, adhesion, colonization, and invasion of Hs832(C).TCs. In the mouse model of endometriosis, we found elevated chemokines (CCL-11, CCL-22 and CXCL13) levels. An increased level of MCP-1 mediated ILK activation, leading to increased inflammatory reaction and infiltration of residential and circulatory macrophages, and monocyte differentiation, but suppressed the anti-inflammatory reaction. The inhibitor (CPD22) of ILK reversed the MCP-1-mediated action by restoring Hs832(C).TCs and THP-1 phenotype. ILK inhibition in a mouse model of endometriosis reduced the effects of MCP-1 mediated pro-inflammatory cytokines, but increased anti-inflammatory response along with T-regulatory and T-helper cell restoration. SIGNIFICANCE: Targeting ILK restores MCP-1 milieu in the peritoneal cavity and endometrial tissues, reduces the inflammatory response, improves the T-regulatory and T-helper cells in the endometriosis mouse model and decreases the migration, adhesion, colonization and invasion of endometriotic cells.

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Condition tags

endometriosis

MeSH descriptors

Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Chemokine CCL2

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (6)

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